THE PROBLEM
Why 70%+ of Solid Tumor Patients Don’t Respond to PD-1 Therapy
The adaptive checkpoint therapies that transformed oncology — anti-PD-1, anti-CTLA-4 — work by re-activating T cells. But in many solid tumors, immune suppression happens earlier, at the innate immune level, before T cells are ever recruited.
Platelets play a central and underappreciated role in this suppression. When activated, platelets release TLT-1 — and we believe this is a key reason why so many tumors remain “cold” and unresponsive to existing immunotherapy.
70%+
Solid tumor patients do not respond to anti-PD-1
30%
Pooled ORR across tumor types for anti-PD-1 monotherapy
$9.5B
Addressable market in mCRC + PROC today, scaling toward $25B+
0
Approved therapies for IO-refractory majority in mCRC MSS patients
THE DISCOVERY
CD11b: A Novel Innate Immune Checkpoint Axis
TLT-1 is a protein secreted almost exclusively by activated platelets. Our research identifies it as a novel innate immune checkpoint — enriched in tumors resistant to anti-PD-1, and correlated with poorer overall survival.
Through mass spectrometry analysis, we identified CD11b (Mac-1, integrin αMβ2) as TLT-1’s binding partner on innate immune cells. This interaction polarizes macrophages toward M2-like, immune-suppressive phenotypes — disarming the innate immune response before it can act.
Published: J Immunol. 2023;210(9):1351–1362.
FROM DISCOVERY TO THE CLINIC
Translating TLT-1/CD11b Science into Two Therapies
Our platform produces two complementary therapeutics from the same biological insight — one targeting cancer, one targeting autoimmune disease.
ASD141 — ONCOLOGY · PHASE I
Anti-CD11b Monoclonal Antibody
Blocks TLT-1/CD11b interaction to remodel the tumor microenvironment and restore innate immune activity. Active in monotherapy and in combination with anti-PD-1 / anti-CTLA-4. Currently in Phase I dose-escalation trials.
ASD001 — AUTOIMMUNE · IND-ENABLING
Anti-CD11b Monoclonal Antibody
Targets CD11b-mediated immune dysregulation. Preclinical data demonstrate efficacy comparable to infliximab in IBD models. IND submission planned for 2027.
Interested in Our Science?
Our scientific team welcomes discussions with potential partners, collaborators, and investors.